Abstract
We characterized the effect of systemic therapy given after portal vein embolization (PVE) and before hepatectomy on hepatic tumor and functional liver remnant (FLR) volumes. All 76 patients who underwent right PVE from 2002–2016 were retrospectively studied. Etiologies included colorectal cancer (n = 44), hepatocellular carcinoma (n = 17), cholangiocarcinoma (n = 10), and other metastases (n = 5). Imaging before and after PVE was assessed. Chart review revealed systemic therapy administration, SNaPshot genetic profiling, and comorbidities. Nine patients received systemic therapy; 67 did not. Tumor volume increased 28% in patients who did not receive and decreased −24% in patients who did receive systemic therapy (p = 0.026), with no difference in FLR growth (28% vs. 34%; p = 0.645). Among 30 patients with genetic profiling, 15 were wild type and 15 had mutations. Mutations were an independent predictor of tumor growth (p = 0.049), but did not impact FLR growth (32% vs. 28%; p = 0.93). Neither cirrhosis, hepatic steatosis, nor diabetes impacted changes in tumor or FLR volume (p > 0.20). Systemic therapy administered after PVE before hepatic lobectomy had no effect on FLR growth; however, it was associated with decreasing tumor volumes. Continuing systemic therapy until hepatectomy may be warranted, particularly in patients with genetic mutations.
Highlights
Portal vein embolization (PVE) is performed before hepatic lobectomy for primary and secondary liver malignancy to increase the size of the functional liver remnant (FLR) to avoid post-hepatectomy failure [1,2]
Patients who did not receive systemic therapy had increased tumor volume (28% ± 13%) whereas patients who received systemic therapy had decreased tumor volume (−24% ± 23%) (p = 0.026)
FLR growth was reduced by a third when chemotherapy was given to patients undergoing PVE for colorectal metastasis [11]
Summary
Portal vein embolization (PVE) is performed before hepatic lobectomy for primary and secondary liver malignancy to increase the size of the functional liver remnant (FLR) to avoid post-hepatectomy failure [1,2]. During the interval between PVE and surgery, tumor growth may occur, and can be mediated by several pathways. The RAS proteins, which are GTPases involved in cell signaling, are among the most common oncogenes, with KRAS mutations determining the response to certain systemic therapies [3]. PI3Ks, intracellular signal transducer enzymes, stimulate RAS pathways.
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